Developmental arrest in response to reduced protein synthesis in C. elegans
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA510325 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8327830_1.fastq.gz | Fastqsanger.gz | |||
| SRR8327830_2.fastq.gz | Fastqsanger.gz | |||
| SRR8327840_1.fastq.gz | Fastqsanger.gz | |||
| SRR8327840_2.fastq.gz | Fastqsanger.gz | |||
| SRR8327831_1.fastq.gz | Fastqsanger.gz |
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Project description:Reducing overall biosynthetic capacity is one avenue for increasing health and lifespan; however, animals must be post-developmental in order to reap these benefits. When protein synthesis is reduced in newly hatched C. elegans, worms enter a temporary arrest state that promotes stress resistance and increases lipid stores. In order to determine the genetic underpinnings to this developmental arrest, we used RNA-seq to determine the transcriptional profile of animals arrested for 48hrs and 120hrs as L2 animals (via egl-45/EIF3A and rps-11/RPS11 RNAi) versus 24hr Control RNAi non-arrested animals. The gene expression differences provide insights into the arrested state and allow for comparison to gene expression changes in adult animals in order to determine if they are activating similar pathways. Better understanding these gene expression changes will allow future research into activating the positive benefits of these pathways independently from any negative consequences of reducing biosynthetic capacity.
2021-12-14 | GSE123921 | GEO
Project description:mRNA-seq analysis of early adult C. elegans fatty acid synthesis mutant following extended L1 arrest
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Project description:mRNA-seq analysis of early adult C. elegans following extended L1 arrest with reduced insulin/insulin-like signaling
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Project description:Metazoan growth and development requires the coordination of cell cycle progression and metabolism with nutrient availability1-3. Here, we show that in C. elegans, amphid neurons regulate the animals’ developmental decision to continue reproductive growth or arrest as quiescent dauer larvae in response to food, by controlling the activity of C. elegans p53-like ortholog, CEP-1. Specifically, upon food availability, larval neurons secrete a mammalian IL-17 ortholog, ILC-17.1, and ILC-17.1 signaling is needed for C. elegans to progress through development into reproductive adults. ILC-17.1 deficiency activates CEP-1/p53 in larval blast cells, and causes larvae to arrest as stress-resistant, quiescent dauers by activating DAF-16/FOXO, decreasing cytochrome C levels, decreasing glucose utilization and upregulating cell cycle inhibitors. Increasing ILC-17.1 levels represses CEP-1/p53 and promotes anabolic growth, but also inhibits apoptosis upon genotoxic stress. IL-17 also represses p53 in human epithelial cells. These studies describe a role for the tumor suppressor p53-like proteins in controlling developmental quiescence of a metazoan in response to neuronal activity and immunometabolic signals and are relevant to our understanding of neuroimmune mechanisms in cancer. This novel role for p53-like proteins in C. elegans supports the argument that their developmental function was a main driving force in their evolution4,5.
2024-01-30 | GSE218596 | GEO
Project description:Flagellar mutants have reduced pilus synthesis in Caulobacter crescentus
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Project description:We characterized the effects of early-life starvation and reduced insulin/insulin-like signaling (IIS) during larval development on adult gene expression using mRNA-seq of whole worms. In our two-factor design, 'starved' worms were cultured without food (E. coli) in L1 arrest for eight days, and 'control' worms were starved overnight for synchronization. Both populations of worms were fed ad libitum with either empty vector (EV; negative control) or daf-2/InsR RNAi food (reduced IIS). RNAi was used rather than a daf-2 mutant so that the results would not be confounded by daf-2 function during L1 arrest, instead disrupting daf-2 only after starvation in fed, developing larvae. Upon reaching adulthood, animals were collected for transcript profiling.
2022-11-08 | GSE178170 | GEO
Project description:Nutritional intake influences animal growth, reproductive capacity, and survival of animals. Under nutrition deficiency, animal developmental arrest occurs as an adaptive strategy to survive. However, the nutritional basis and the underlying nutrient sensing mechanism essential for animal regrowth after developmental arrest remain to be explored. In Caenorhabditis elegans, larvae undergo early developmental arrest are stress resistant, and they require certain nutrients to recover postembryonic development. Here, we investigated the developmental arrest in C. elegans feeding on Lactiplantibacillus plantarum, and the rescue of the diapause state with trace supplementation of Escherichia coli. We performed a genome-wide screen using 3983 individual gene deletion E. coli mutants and identified E. coli genes that are indispensable for C. elegans larval growth on originally not nutritionally sufficient bacteria L. plantarum. Among these crucial genes, we confirmed E. coli pdxH, and the downstream metabolite pyridoxal 5-P (PLP, Vitamin B6) as important nutritional factors for C. elegans postembryonic development. Transcriptome results suggest that bacterial pdxH affects host development by coordinating host metabolic processes and PLP binding. Additionally, the developmental arrest induced by the L. plantarum diet in worm does not depend on the activation of FoxO/DAF-16. Altogether, these results highlight the role of microbial metabolite PLP as a crucial cofactor to restore postembryonic development in C. elegans.
2024-02-23 | GSE254343 | GEO
Project description:Insulin and insulin-like growth factor signalling regulates a broad spectrum of growth and metabolic responses to a variety of internal and environmental stimuli. Such responses can be tailored so that changes in insulin signalling result in distinct physiological responses to different stimuli. For example, the inhibition of insulin-like signalling is key in the responses of the nematode C. elegans to both osmotic stress and starvation, but these two stresses result in responses that are both physiologically and molecularly distinct. How does reduced insulin-like signalling elicit different responses to different environmental stimuli? We report that neurohormonal signalling involving the C. elegans cytosolic sulfotransferase SSU-1 controls developmental arrest in response to osmotic stress but does not control the distinct developmental arrest that occurs in response to starvation. SSU-1 functions in a single pair of sensory neurons to control intercellular signalling -- likely by catalyzing the synthesis of a steroid hormone -- via the nuclear hormone receptor NHR-1. SSU-1-controlled signalling antagonizes insulin-like signalling and hence modulates insulin sensitivity. In short, we describe a previously unknown neurohormonal signalling pathway that is required specifically for some but not all consequences of reduced insulin-like signalling. In mammals, the nervous system plays a similarly important yet poorly understood role in modulating insulin sensitivity. Our results suggest that the mammalian nervous system might regulate insulin sensitivity via sulfotransferase-controlled neurohormonal signalling.
2018-10-14 | GSE111074 | GEO
Project description:Developmental dynamics of C. elegans dosage compensation
| PRJNA280541 | ENA
Project description:Diapause is a reversible developmental arrest faced by many organisms in harsh environments. Annual killifish present this mechanism in three possible stages of development. Killifish are freshwater teleosts from Africa and America that live in ephemeral ponds, which dry up in the dry season. The juvenile and adult populations die, and the embryos remain buried in the bottom mud until the next rainy season. Thus, species survival is entirely embryo-dependent, and they are perhaps the most remarkable extremophile organisms among vertebrates. The aim of the present study was to gather information about embryonic diapauses with the use of a “shotgun” proteomics approach in diapause III and prehatching Austrolebias charrua embryos. Our results provide insight into the molecular mechanisms of diapause III. We detected a diapause-dependent change in a large group of proteins involved in different functions, such as metabolic pathways and stress tolerance, as well as proteins related to DNA repair and epigenetic modifications. Furthermore, we observed a diapauseassociated switch in cytoskeletal proteins. This first glance into global protein expression differences between prehatching and diapause III could provide clues regarding the induction/maintenance of this developmental arrest in A. charrua embryos. There appears to be no single mechanism underlying diapause and the present data expand our knowledge of the molecular basis of diapause regulation. This information will be useful for future comparative approaches among different diapauses in annual killifish and/or other organisms that experience developmental arrest.
2021-05-12 | PXD025196 | Pride